Faculty Bibliography

Background and Purpose/UNASSIGNED:The ideal dosing regimen of 4-factor prothrombin complex concentrate (4FPCC) after warfarin-induced intracranial hemorrhage (WICH) remains unclear. We sought to compare the safety and efficacy of the 4FPCC package insert dosing strategy (standard dose [SD]) with our institutional guideline for high-dose (HD) 4FPCC for patients with WICH. Methods/UNASSIGNED:We compared the percentage of SD and HD patients who achieved an international normalized ratio (INR) ≤1.3 at a single institution between January 2014 and July 2017. Additionally, we assessed hematoma expansion, recurrence of INR > 1.3, and occurrence of thrombotic events within 7 days of 4FPCC administration. Results/UNASSIGNED:= .243). Conclusions/UNASSIGNED:High-dose 4FPCC appears to be more effective at lowering INR and preventing bleed expansion in patients with WICH, while maintaining a similar safety profile.

Over 115 000 people are waiting for life-saving organ transplants, of whom a small fraction will receive transplants and many others will die while waiting. Existing efforts to expand the number of available organs, including increasing the number of registered donors and procuring organs in uncontrolled environments, are crucial but unlikely to address the shortage in the near future and will not improve donor/recipient compatibility or organ quality. If successful, organ bioengineering can solve the shortage and improve functional outcomes. Studying manufactured organs in animal models has produced valuable data, but is not sufficient to understand viability in humans. Before risking manufactured organ experimentation in living humans, study of bioengineered organs in recently deceased humans would facilitate evaluation of the function of engineered tissues and the complex interactions between the host and the transplanted tissue. Although such studies do not pose risk to human subjects, they pose unique ethical challenges concerning the previous wishes of the deceased, rights of surviving family members, effective operation and fair distribution of medical services, and public transparency. This article investigates the ethical, legal and social considerations in performing engineered organ research on the recently deceased.

Introduction Tranexamic Acid (TXA) is an intravenous antifibrinolytic agent that is used routinely for elective surgery. We report a case of inadvertent intrathecal injection of TXA resulting in refractory status epilepticus. Methods Case report. Results A 71-year-old healthy female admitted for bilateral total knee replacement was inadvertently administered 300mg of TXA intrathecally instead of bupivacaine. Soon after administration, she developed myoclonic jerking. When the error was identified, 15cc of CSF was removed. She was intubated, administered levetiracetam, started on a propofol infusion, and transferred to the neurointensive care unit (NICU). She developed persistent spontaneous and stimulus induced generalized myoclonus refractory to propofol. Midazolam infusion was added. NCHCT and CTA demonstrated pneumocephalus, but no acute arterial or venous thrombosis or stroke. vEEG revealed generalized nonconvulsive seizures occurring once per minute, not correlating with spinal myoclonus . Propofol and midazolam infusions were increased to 150 mcg/kg/min and 2.6 mg/kg/hr, respectively, to achieve burst suppression, and valproic acid was added. Over the following week, the drips were adjusted to suppress seizure activity. By hospital day 8, she was weaned off all infusions without recurrence of seizures. By hospital day 19, she was on levetiracetam monotherapy. She was discharged to rehab after a 22-day hospital course, and was discharged home 45 days after initial presentation. Residual deficits at the time of discharge included mild cognitive impairment and gait instability. She remains seizure-free since hospital day 45 on levetiracetam 500mg BID. Conclusions We report a case of refractory status epilepticus and spinal myoclonus after accidental intrathecal TXA administration. With aggressive management, the patient survived with mild residual deficits. The mechanism by which TXA causes status epilepticus and spinal myoclonus is hypothesized to be related to its inhibitory effects on GABA and glycine receptors, respectively